Abstract
Changes produced in the posterior papillary muscle of the dog following 40 minutes of circumflex artery occlusion and 0 to 20 minutes of blood reflow were studied by electron miroscopy. With no reflow of blood, myocardial cells were modestly swollen, contained amorphous matrix densities in the mitochondria, had aggregation and margination of nuclear chromatin and relaxation of myofibrils. With as little as 2 minutes of blood reflow, cells developed contraction bands and were greatly swollen due to a generalized increase in sarcoplasmic space, formation of vacuoles and swelling of mitochondria. Frequently, cell membranes were lifted away from the myofibers, forming large subsarcolemmal blebs which appeared capable of compressing adjacent capillaries. The extracellular space did not appear to be enlarged, and the marked tissue edema found after reflow was due primarily to accumulation of intracellular fluid. In addition to explosive cell swelling, there was, over the 2- to 20-minute period of reflow, a progressive increase in size and number of granular mitochondrial dense bodies of the calcium accumulation type. No significant changes in lysosomes were observed. The speed with which the morphologic changes developed during very early reflow periods suggests that irreversible ischemic injury produces a defect in cell volume regulation during the phase of ischemia and that this defect becomes manifest if arterial flow is restored to the affected cells.
MeSH Terms
Animals
Calcium/metabolism
Cell Membrane Permeability
Chromatin
Coronary Circulation
Dogs
Edema/pathology
Female
Ischemia/pathology
Lysosomes
Male
Microcirculation
Microscopy, Electron
Mitochondrial Swelling
Myocardial Infarction/metabolism,pathology
Myocardium/metabolism,pathology
Myofibrils
Papillary Muscles/pathology
Sarcolemma
Time Factors
Water-Electrolyte Balance
Chemicals
Chromatin
Calcium
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Kloner R A
Ganote C E
Whalen D A
Jennings R B
References (26)
26 references, click to expand
-
Regulation of intracellular fluid volume and disease.
Am J Med. 1970 Sep;49(3):291-5
PMID: 5455560
-
The no reflow phenomenon in renal ischemia.
Lab Invest. 1971 Dec;25(6):635-43
PMID: 5129762
-
Experimental prevention of cerebral vasculature obstruction produced by ischemia.
J Neurosurg. 1969 Jan;30(1):50-4
PMID: 5766615
-
Myocardial lysosome stability in the early stages of acute ischemic injury.
Am J Cardiol. 1972 Oct;30(5):492-7
PMID: 5073661
-
Structural and functional abnormalities in mitochondria isolated from ischemic dog myocardium.
Lab Invest. 1969 Jun;20(6):548-57
PMID: 4306675
-
Cellular death and necrosis: chemical, physical and morphologic changes in rat liver.
Virchows Arch Pathol Anat Physiol Klin Med. 1960;333:421-65
PMID: 13765553
-
Lysosomes and myocardial cellular injury.
Am J Cardiol. 1972 Oct;30(5):498-502
PMID: 5073662
-
A COMPARATIVE STUDY OF THE FINE STRUCTURE OF NORMAL AND ISCHEMIC DOG MYOCARDIUM WITH SPECIAL REFERENCE TO EARLY CHANGES FOLLOWING TEMPORARY OCCLUSION OF A CORONARY ARTERY.
Am J Pathol. 1965 Mar;46:367-86
PMID: 14266217
-
Cerebral ischemia. I. An improved experimental method for study; cardiovascular effects and demonstration of an early vascular lesion in the rabbit.
J Neurosurg. 1968 Feb;28(2):150-7
PMID: 5638013
-
Lysosome and phagosome stability in lethal cell injury. Morphologic tracer studies in cell injury due to inhibition of energy metabolism, immune cytolysis and photosensitization.
Am J Pathol. 1972 Aug;68(2):255-8
PMID: 4340333
-
Contributions of electron microscopy to the study of myocardial ischaemia.
Bull World Health Organ. 1969;41(6):865-72
PMID: 4908552
-
Myocardial ischemia and early infarction: an electron microscopic study.
Am J Pathol. 1959 May-Jun;35(3):489-523
PMID: 13649884
-
Myocardial necrosis induced by temporary occlusion of a coronary artery in the dog.
Arch Pathol. 1960 Jul;70:68-78
PMID: 14407094
-
Blood supply of the myocardium after temporary coronary occlusion.
Circ Res. 1966 Jul;19(1):57-62
PMID: 5912914
-
EXPERIMENTAL ACUTE MYOCARDIAL INFARCTION; HISTOLOGIC AND HISTOCHEMICAL STUDIES OF EARLY MYOCARDIAL INFARCTS INDUCED BY TEMPORARY OR PERMANENT OCCLUSION OF A CORONARY ARTERY.
Lab Invest. 1964 Dec;13:1491-503
PMID: 14252312
-
The role of cell swelling in ischemic renal damage and the protective effect of hypertonic solute.
J Clin Invest. 1972 Jan;51(1):118-26
PMID: 5007042
-
Kinetics of calcium accumulation in acute myocardial ischemic injury.
Am J Pathol. 1972 Jun;67(3):441-52
PMID: 5033258
-
STUDIES ON ION TRANSPORT. III. THE ACCUMULATION OF CALCIUM AND INORGANIC PHOSPHATE BY HEART MITOCHONDRIA.
Arch Biochem Biophys. 1964 Apr;105:89-102
PMID: 14165509
-
Effect of a transient period of ischemia on myocardial cells. I. Effects on cell volume regulation.
Am J Pathol. 1974 Mar;74(3):381-97
PMID: 4814894
-
The mechanism of muscular contraction.
Science. 1969 Jun 20;164(3886):1356-65
PMID: 4181952
-
FINE STRUCTURAL CHANGES IN MYOCARDIAL ISCHEMIC INJURY.
Arch Pathol. 1965 Feb;79:135-43
PMID: 14232929
-
Production of an area of homogeneous myocardial infarction in the dog.
AMA Arch Pathol. 1957 Jun;63(6):580-5
PMID: 13423975
-
The extent of ischemic damage in the myocardium of the cat after permanent and temporary coronary occlusion.
J Thorac Cardiovasc Surg. 1970 Aug;60(2):242-7
PMID: 4194890
-
Myocardial calcium and magnesium in acute ischemic injury.
Am J Pathol. 1972 Jun;67(3):417-40
PMID: 5033257
-
Cerebral ischemia. III. Vascular changes.
Am J Pathol. 1968 Feb;52(2):455-76
PMID: 5635862
-
Ischemic injury of myocardium.
Ann N Y Acad Sci. 1969 Jan 31;156(1):61-78
PMID: 5291154